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10.1038/s41467-021-21289-y

http://scihub22266oqcxt.onion/10.1038/s41467-021-21289-y
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33597532!7889643!33597532
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suck abstract from ncbi


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pmid33597532      Nat+Commun 2021 ; 12 (1): 1079
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  • Dysregulated transcriptional responses to SARS-CoV-2 in the periphery #MMPMID33597532
  • McClain MT; Constantine FJ; Henao R; Liu Y; Tsalik EL; Burke TW; Steinbrink JM; Petzold E; Nicholson BP; Rolfe R; Kraft BD; Kelly MS; Saban DR; Yu C; Shen X; Ko EM; Sempowski GD; Denny TN; Ginsburg GS; Woods CW
  • Nat Commun 2021[Feb]; 12 (1): 1079 PMID33597532show ga
  • SARS-CoV-2 infection has been shown to trigger a wide spectrum of immune responses and clinical manifestations in human hosts. Here, we sought to elucidate novel aspects of the host response to SARS-CoV-2 infection through RNA sequencing of peripheral blood samples from 46 subjects with COVID-19 and directly comparing them to subjects with seasonal coronavirus, influenza, bacterial pneumonia, and healthy controls. Early SARS-CoV-2 infection triggers a powerful transcriptomic response in peripheral blood with conserved components that are heavily interferon-driven but also marked by indicators of early B-cell activation and antibody production. Interferon responses during SARS-CoV-2 infection demonstrate unique patterns of dysregulated expression compared to other infectious and healthy states. Heterogeneous activation of coagulation and fibrinolytic pathways are present in early COVID-19, as are IL1 and JAK/STAT signaling pathways, which persist into late disease. Classifiers based on differentially expressed genes accurately distinguished SARS-CoV-2 infection from other acute illnesses (auROC 0.95 [95% CI 0.92-0.98]). The transcriptome in peripheral blood reveals both diverse and conserved components of the immune response in COVID-19 and provides for potential biomarker-based approaches to diagnosis.
  • |COVID-19/blood/*genetics/virology[MESH]
  • |Cytokines/genetics[MESH]
  • |Gene Expression Profiling/*methods[MESH]
  • |Host-Pathogen Interactions[MESH]
  • |Humans[MESH]
  • |Influenza, Human/genetics[MESH]
  • |Leukocytes, Mononuclear/*metabolism[MESH]
  • |Pneumonia, Bacterial/genetics[MESH]
  • |SARS-CoV-2/physiology[MESH]
  • |Sequence Analysis, RNA/*methods[MESH]
  • |Signal Transduction/genetics[MESH]


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